Posttraumatic Stress Disorder (PTSD) is common in Veterans and associated with a number of negative physical and mental health consequences. While evidence-based pharmacological and psychosocial interventions for PTSD have been developed, not all patients respond fully to treatment. Investigating the biological processes involved in the development and maintenance of PTSD will increase understanding of the disorder and aid in the development of more effective interventions. Sleep disruption, particularly Rapid Eye Movement (REM) sleep disruption, is a potent and modifiable risk factor contributing to PTSD. For example, longitudinal studies have shown REM sleep fragmentation in the acute aftermath of trauma predicts PTSD symptoms at a later timepoint, underscoring the potential importance of sleep as a mechanism in PTSD. Recent research has also demonstrated an association between poor sleep and impaired emotion regulation. Specifically, research suggests disrupted sleep impairs effective emotion regulation strategies, such as cognitive reappraisal, while increasing reliance on more maladaptive emotion regulation strategies, such as expressive suppression. For example, previous studies have shown poor sleep at baseline predicts impaired cognitive reappraisal in lab-based tasks involving emotionally provocative stimuli. Our research group has also demonstrated that poor self-reported global sleep quality is associated with reduced cognitive reappraisal and increased reliance on expressive suppression when measured at one timepoint in a large group of Veterans with and without PTSD. The implications of this finding are particularly salient for patients with PTSD, because maladaptive emotion regulation contributes to severity of trauma-related symptoms, increases distress, and interferes with gold-standard interventions for PTSD. However, most research linking disrupted sleep to impaired emotion regulation has been conducted in healthy controls, or at only one time-point in clinical samples. Therefore, additional research is necessary to provide support for a hypothesized model whereby disrupted sleep contributes to maladaptive emotion regulation, thus in turn maintaining trauma-related symptoms. This study responds to these gaps in the literature by using both self-report longitudinal measures and an experimental sleep manipulation to test the hypothesis that disrupted sleep contributes to maladaptive emotion regulation in Veterans with and without PTSD. The first aim of the study will be to examine whether poor sleep at one timepoint predicts maladaptive emotion regulation and trauma-related symptoms at subsequent timepoints in a large cohort of Veterans with and without PTSD. The Insomnia Severity Index (ISI), the Emotion Regulation Questionnaire (ERQ), and the PTSD Checklist (PCL) will be measured at three timepoints in this cohort. We hypothesize that poor sleep at the first timepoint will predict reduced reappraisal, increased expressive suppression, and increased severity of trauma-related symptoms at the subsequent timepoints. The second portion of the proposed project will build upon these findings by experimentally testing the notion that disrupted sleep results in impaired emotion regulation, and will also directly test the hypothesis that REM sleep specifically is tied to emotion regulation processes. A sample of Veterans (n = 60) with and without PTSD will be recruited and randomized to undergo one of three sleep conditions: 1) one night of REM sleep deprivation (REMD), 2) one night of slow-wave sleep deprivation (SWSD, an active control condition), or 3) one night of normal sleep. Participants will then participate in two laboratory emotion reappraisal tasks using images from the International Affective Picture System (IAPS). We hypothesize that participants in the REMD group will rate the images more negatively during a cognitive reappraisal task than SWSD group or the normal sleep group, and will also be more likely to choose expressive suppression than reappraisal on an emotion regulation choice task. Exploratory analyses will determine if this effect differs by diagnostic group status.